Skip to main content
. 2012 Apr 23;14(3):465–475. doi: 10.1038/aja.2012.20

Figure 3.

Figure 3

Representative factors found in the epididymis that are involved in pro-cancer and tumour suppression mechanisms in cancer-prone tissues. Tumours follow transformation of a susceptible cell type to a potentially cancerous form (via proliferation) that can either be suppressed (immune suppression) or remain dormant until conditions allow progression into malignant tissues (by immune escape). Pro-cancer forces are shown in red; anti-cancer in green. Boxed factors are constitutively expressed in the epididymis, but only upregulated in cancer cells upon induction by pro-tumour factors. Circled factors are in the epididymal epithelium but not localized where they are in cancerous tissues. Square brackets enclose factors that have not been proven to be in the epididymis or non-endogenous factors that have been used to drive tumourigenesis. Factors not in parentheses are present in the epididymis as RNA or protein (see text for details). The major causes of tumourigenicity, ROS and oncogene expression, are either heavily suppressed or inoperative, respectively. There is no evidence that the boxed factors elicit the responses that occur in cancer-prone tissues. Even when induction of tumourigenesis is attempted (e.g., by introduction of SV40 or driving exogenous oncogenes by MTV or LPK), no progression beyond epididymal hyperplasia occurs, suggesting that immunosurveillance maintains the tissue in a dormant state. Bcl-2, B-cell lymphoma-2; β-CAT, beta-catenin; β-Gal, beta-galactosidase; CA2,9, carbonic anhydrase 2,9; CAT, catalase; Cath-D, cathepsin D; CD4T/8T, CD4-/8-positive T-lymphocytes; CEACAM1, carcino-embryonic antigen-related cell adhesion molecule; DC, dendritic cells; DUSP6, dual-specificity phosphatise 6; Fas, Fas receptor CD95; FasL, Fas ligand CD95L; Glut1, glucose transporter 1; GPX, glutathione peroxidases; GR, glutathione reductase; GSH, glutathione; GST, glutathione S-transferase; HIF, hypoxia-induced factor; IDO, indoleamine 2,3-dioxygenase; INF-γ, interferon gamma; LPK, L-type pyruvate kinase gene promoter; MMP7, matrix metalloproteinase 7 (matrilysin); MTV, mouse mammary tumour virus long terminal repeat; NHE, sodium-hydrogen exchanger; Nrf2, nuclear factor E2-related factor 2; NK, natural killer cells; NKT, natural killer T-lymphocytes; p53, tumour suppressor protein 53; pCO2↑, high tissue carbon dioxide; PDGF, platelet-derived growth factor; pHe↓, high extra-cellular acidity; pO2↓, low tissue oxygen tension; PRDX, peroxiredoxins; ROS, reactive oxygen species; SABG, senescence-associated beta-galactosidase; SED1, secreted protein 1 with two EGF repeats and discoidin domains; SOD, superoxide dismutase; SV40, Simian virus 40 large T antigen; TGF-β, transforming growth factor beta; TRX, thioredoxin peroxidases; VA, vacuolar ATPase; VEGF, vascular endothelial growth factor; VEGF-R, VEFG receptor; Wnt, Wingless/int pro-tumour protein; φ, macrophage.